BEGIN:VCALENDAR
PRODID:-//Columba Systems Ltd//NONSGML CPNG/SpringViewer/ICal Output/3.3-
 M3//EN
VERSION:2.0
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VEVENT
DTSTAMP:20141028T125213Z
DTSTART:20141111T130000Z
DTEND:20141111T140000Z
SUMMARY:Nrf2 and miR-29s regulate desmosome function in keratinocytes
UID:{http://www.columbasystems.com/customers/uom/gpp/eventid/}adi-i1nfeu2
 3-mqsume
DESCRIPTION:This seminar is part of the Tissue Systems seminar series.   
                                                                         
                                                       miRNAs are small R
 NA molecules implicated in skin homeostasis and repair\; however\, very 
 little is known about mechanisms that regulate expression and function o
 f miRNAs in epidermis during normal differentiation and in skin patholog
 y. Recently\, our group had identified miR-29a and miR-29b as regulators
  of desmosome function in keratinocytes in vivo. Increase in miR-29s dow
 nregulted desmosomal cadherin Dsc2 and impaired formation of desmosomes.
  In vivo\, enhanced expression of miR-29 and decreased Dsc2 levels were 
 observed in the epidermis of mice with constitutively active Nrf2\, whic
 h was accompanied by structural alterations of the epidermal desmosomes 
 and impairments of the epidermal barrier. We identified two gene cluster
 s encoding for miR-29s as novel direct targets of Nrf2 in the epidermis 
 and found a molecular mechanism of transcriptional regulation of miR-29 
 genes. These mechanisms are conserved in human keratinocytes where Nrf2 
 activates MIR29AB1 gene\, and DNA methylation silences MIR29B2C. These r
 esults identified a novel Nrf2-miR-29-Dsc2 axis controlling desmosome fo
 rmation and cutaneous homeostasis. Expanding on the mechanisms of miR-29
 s upregulation in vivo will lead to the clinical use of miR-29 mimics an
 d antagomiRs to control skin regeneration and disease.
STATUS:TENTATIVE
TRANSP:TRANSPARENT
CLASS:PUBLIC
LOCATION:Lecture Theatre\, Michael Smith Building\, Manchester
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